StressCovidV1, Main, Exploration, bibRecord, 000B96

Avenues to autoimmune arthritis triggered by diverse remote inflammatory challenges.

Identifieur interne : 000B96 ( Main/Exploration ); précédent : 000B95; suivant : 000B97

Avenues to autoimmune arthritis triggered by diverse remote inflammatory challenges.

Auteurs : Nina Chevalier [Australie] ; Jian K. Tan [Australie] ; Linda J. Mason [Australie] ; Remy Robert [Australie] ; Craig I. Mckenzie [Australie] ; Florence Lim [Australie] ; Connie H. Wong [Australie] ; Laurence Macia [Australie] ; Alison N. Thorburn [Australie] ; Brendan E. Russ [Australie] ; Seth L. Masters [Australie] ; Charles R. Mackay [Australie]

Source :

Journal of autoimmunity [ 1095-9157 ] ; 2016.

RBID : pubmed:27427404

Descripteurs français

English descriptors

KwdEn :
- Adoptive Transfer, Animals, Arthritis, Experimental (immunology), Arthritis, Rheumatoid (genetics), Arthritis, Rheumatoid (immunology), CD4-Positive T-Lymphocytes (immunology), Cell Differentiation (immunology), Colitis (chemically induced), Colitis (immunology), Dextran Sulfate (toxicity), Genetic Predisposition to Disease, Influenza A virus (immunology), Interleukin-17 (metabolism), Interleukin-1beta (metabolism), Joints (immunology), Klebsiella pneumoniae (immunology), Lung Diseases (immunology), Lung Diseases (virology), Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Transgenic, Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (virology), Pneumonia, Bacterial (immunology), Pneumonia, Bacterial (microbiology), Receptors, Interleukin-1 (genetics), Receptors, Interleukin-1 (metabolism), Spondylarthritis (immunology), Th17 Cells (immunology), Th17 Cells (metabolism).
MESH :
- chemical , genetics : Receptors, Interleukin-1.
- chemical , metabolism : Interleukin-17, Interleukin-1beta, Receptors, Interleukin-1.
- chemical , toxicity : Dextran Sulfate.
- chemically induced : Colitis.
- genetics : Arthritis, Rheumatoid.
- immunology : Arthritis, Experimental, Arthritis, Rheumatoid, CD4-Positive T-Lymphocytes, Cell Differentiation, Colitis, Influenza A virus, Joints, Klebsiella pneumoniae, Lung Diseases, Orthomyxoviridae Infections, Pneumonia, Bacterial, Spondylarthritis, Th17 Cells.
- metabolism : Th17 Cells.
- microbiology : Pneumonia, Bacterial.
- virology : Lung Diseases, Orthomyxoviridae Infections.
- Adoptive Transfer, Animals, Genetic Predisposition to Disease, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Transgenic.

Abstract

Environmental factors contribute to development of autoimmune diseases. For instance, human autoimmune arthritis can associate with intestinal inflammation, cigarette smoking, periodontal disease, and various infections. The cellular and, molecular pathways whereby such remote challenges might precipitate arthritis or flares remain unclear. Here, we used a transfer model of self-reactive arthritis-inducing CD4(+) cells from KRNtg mice that, upon transfer, induce a very mild form of autoinflammatory arthritis in recipient animals. This model enabled us to identify external factors that greatly aggravated disease. We show that several distinct challenges precipitated full-blown arthritis, including intestinal inflammation through DSS-induced colitis, and bronchial stress through Influenza infection. Both triggers induced strong IL-17 expression primarily in self-reactive CD4(+) cells in lymph nodes draining the site of inflammation. Moreover, treatment of mice with IL-1β greatly exacerbated arthritis, while transfer of KRNtg CD4(+) cells lacking IL-1R significantly reduced disease and IL-17 expression. Thus, IL-1β enhances the autoaggressive potential of self-reactive CD4(+) cells, through increased Th17 differentiation, and this influences inflammatory events in the joints. We propose that diverse challenges that cause remote inflammation (lung infection or colitis, etc.) result in IL-1β-driven Th17 differentiation, and this precipitates arthritis in genetically susceptible individuals. Thus the etiology of autoimmune inflammatory arthritis likely relates to diverse triggers that converge to a common pathway involving IL-1β production and Th17 cell distribution.

DOI: 10.1016/j.jaut.2016.06.018
PubMed: 27427404

Affiliations:

Le document en format XML

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<author><name sortKey="Wong, Connie H" sort="Wong, Connie H" uniqKey="Wong C" first="Connie H" last="Wong">Connie H. Wong</name>
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<country xml:lang="fr">Australie</country>
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<author><name sortKey="Macia, Laurence" sort="Macia, Laurence" uniqKey="Macia L" first="Laurence" last="Macia">Laurence Macia</name>
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<country xml:lang="fr">Australie</country>
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<author><name sortKey="Thorburn, Alison N" sort="Thorburn, Alison N" uniqKey="Thorburn A" first="Alison N" last="Thorburn">Alison N. Thorburn</name>
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<country xml:lang="fr">Australie</country>
<wicri:regionArea>Infection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, 3800 VIC</wicri:regionArea>
<wicri:noRegion>3800 VIC</wicri:noRegion>
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<author><name sortKey="Russ, Brendan E" sort="Russ, Brendan E" uniqKey="Russ B" first="Brendan E" last="Russ">Brendan E. Russ</name>
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<country xml:lang="fr">Australie</country>
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<region type="état">Victoria (État)</region>
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<orgName type="university">Université de Melbourne</orgName>
<placeName><settlement type="city">Melbourne</settlement>
<region type="état">Victoria (État)</region>
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<author><name sortKey="Masters, Seth L" sort="Masters, Seth L" uniqKey="Masters S" first="Seth L" last="Masters">Seth L. Masters</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adoptive Transfer</term>
<term>Animals</term>
<term>Arthritis, Experimental (immunology)</term>
<term>Arthritis, Rheumatoid (genetics)</term>
<term>Arthritis, Rheumatoid (immunology)</term>
<term>CD4-Positive T-Lymphocytes (immunology)</term>
<term>Cell Differentiation (immunology)</term>
<term>Colitis (chemically induced)</term>
<term>Colitis (immunology)</term>
<term>Dextran Sulfate (toxicity)</term>
<term>Genetic Predisposition to Disease</term>
<term>Influenza A virus (immunology)</term>
<term>Interleukin-17 (metabolism)</term>
<term>Interleukin-1beta (metabolism)</term>
<term>Joints (immunology)</term>
<term>Klebsiella pneumoniae (immunology)</term>
<term>Lung Diseases (immunology)</term>
<term>Lung Diseases (virology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Inbred NOD</term>
<term>Mice, Transgenic</term>
<term>Orthomyxoviridae Infections (immunology)</term>
<term>Orthomyxoviridae Infections (virology)</term>
<term>Pneumonia, Bacterial (immunology)</term>
<term>Pneumonia, Bacterial (microbiology)</term>
<term>Receptors, Interleukin-1 (genetics)</term>
<term>Receptors, Interleukin-1 (metabolism)</term>
<term>Spondylarthritis (immunology)</term>
<term>Th17 Cells (immunology)</term>
<term>Th17 Cells (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Arthrite expérimentale (immunologie)</term>
<term>Articulations (immunologie)</term>
<term>Cellules Th17 (immunologie)</term>
<term>Cellules Th17 (métabolisme)</term>
<term>Colite ()</term>
<term>Colite (immunologie)</term>
<term>Différenciation cellulaire (immunologie)</term>
<term>Infections à Orthomyxoviridae (immunologie)</term>
<term>Infections à Orthomyxoviridae (virologie)</term>
<term>Interleukine-1 bêta (métabolisme)</term>
<term>Interleukine-17 (métabolisme)</term>
<term>Klebsiella pneumoniae (immunologie)</term>
<term>Lymphocytes T CD4+ (immunologie)</term>
<term>Maladies pulmonaires (immunologie)</term>
<term>Maladies pulmonaires (virologie)</term>
<term>Pneumopathie bactérienne (immunologie)</term>
<term>Pneumopathie bactérienne (microbiologie)</term>
<term>Polyarthrite rhumatoïde (génétique)</term>
<term>Polyarthrite rhumatoïde (immunologie)</term>
<term>Prédisposition génétique à une maladie</term>
<term>Récepteurs à l'interleukine-1 (génétique)</term>
<term>Récepteurs à l'interleukine-1 (métabolisme)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris de lignée NOD</term>
<term>Souris transgéniques</term>
<term>Spondylarthrite (immunologie)</term>
<term>Sulfate dextran (toxicité)</term>
<term>Transfert adoptif</term>
<term>Virus de la grippe A (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Interleukin-1</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interleukin-17</term>
<term>Interleukin-1beta</term>
<term>Receptors, Interleukin-1</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Dextran Sulfate</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Colitis</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Arthritis, Rheumatoid</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Polyarthrite rhumatoïde</term>
<term>Récepteurs à l'interleukine-1</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Arthrite expérimentale</term>
<term>Articulations</term>
<term>Cellules Th17</term>
<term>Colite</term>
<term>Différenciation cellulaire</term>
<term>Infections à Orthomyxoviridae</term>
<term>Klebsiella pneumoniae</term>
<term>Lymphocytes T CD4+</term>
<term>Maladies pulmonaires</term>
<term>Pneumopathie bactérienne</term>
<term>Polyarthrite rhumatoïde</term>
<term>Spondylarthrite</term>
<term>Virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Arthritis, Experimental</term>
<term>Arthritis, Rheumatoid</term>
<term>CD4-Positive T-Lymphocytes</term>
<term>Cell Differentiation</term>
<term>Colitis</term>
<term>Influenza A virus</term>
<term>Joints</term>
<term>Klebsiella pneumoniae</term>
<term>Lung Diseases</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumonia, Bacterial</term>
<term>Spondylarthritis</term>
<term>Th17 Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Th17 Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Pneumopathie bactérienne</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Pneumonia, Bacterial</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules Th17</term>
<term>Interleukine-1 bêta</term>
<term>Interleukine-17</term>
<term>Récepteurs à l'interleukine-1</term>
</keywords>
<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Sulfate dextran</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à Orthomyxoviridae</term>
<term>Maladies pulmonaires</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung Diseases</term>
<term>Orthomyxoviridae Infections</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adoptive Transfer</term>
<term>Animals</term>
<term>Genetic Predisposition to Disease</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Inbred NOD</term>
<term>Mice, Transgenic</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Colite</term>
<term>Prédisposition génétique à une maladie</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris de lignée NOD</term>
<term>Souris transgéniques</term>
<term>Transfert adoptif</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Environmental factors contribute to development of autoimmune diseases. For instance, human autoimmune arthritis can associate with intestinal inflammation, cigarette smoking, periodontal disease, and various infections. The cellular and, molecular pathways whereby such remote challenges might precipitate arthritis or flares remain unclear. Here, we used a transfer model of self-reactive arthritis-inducing CD4(+) cells from KRNtg mice that, upon transfer, induce a very mild form of autoinflammatory arthritis in recipient animals. This model enabled us to identify external factors that greatly aggravated disease. We show that several distinct challenges precipitated full-blown arthritis, including intestinal inflammation through DSS-induced colitis, and bronchial stress through Influenza infection. Both triggers induced strong IL-17 expression primarily in self-reactive CD4(+) cells in lymph nodes draining the site of inflammation. Moreover, treatment of mice with IL-1β greatly exacerbated arthritis, while transfer of KRNtg CD4(+) cells lacking IL-1R significantly reduced disease and IL-17 expression. Thus, IL-1β enhances the autoaggressive potential of self-reactive CD4(+) cells, through increased Th17 differentiation, and this influences inflammatory events in the joints. We propose that diverse challenges that cause remote inflammation (lung infection or colitis, etc.) result in IL-1β-driven Th17 differentiation, and this precipitates arthritis in genetically susceptible individuals. Thus the etiology of autoimmune inflammatory arthritis likely relates to diverse triggers that converge to a common pathway involving IL-1β production and Th17 cell distribution.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
</country>
<region><li>Nouvelle-Galles du Sud</li>
<li>Victoria (État)</li>
</region>
<settlement><li>Melbourne</li>
<li>Sydney</li>
</settlement>
<orgName><li>Université de Melbourne</li>
</orgName>
</list>
<tree><country name="Australie"><region name="Nouvelle-Galles du Sud"><name sortKey="Chevalier, Nina" sort="Chevalier, Nina" uniqKey="Chevalier N" first="Nina" last="Chevalier">Nina Chevalier</name>
</region>
<name sortKey="Lim, Florence" sort="Lim, Florence" uniqKey="Lim F" first="Florence" last="Lim">Florence Lim</name>
<name sortKey="Macia, Laurence" sort="Macia, Laurence" uniqKey="Macia L" first="Laurence" last="Macia">Laurence Macia</name>
<name sortKey="Mackay, Charles R" sort="Mackay, Charles R" uniqKey="Mackay C" first="Charles R" last="Mackay">Charles R. Mackay</name>
<name sortKey="Mason, Linda J" sort="Mason, Linda J" uniqKey="Mason L" first="Linda J" last="Mason">Linda J. Mason</name>
<name sortKey="Masters, Seth L" sort="Masters, Seth L" uniqKey="Masters S" first="Seth L" last="Masters">Seth L. Masters</name>
<name sortKey="Mckenzie, Craig I" sort="Mckenzie, Craig I" uniqKey="Mckenzie C" first="Craig I" last="Mckenzie">Craig I. Mckenzie</name>
<name sortKey="Robert, Remy" sort="Robert, Remy" uniqKey="Robert R" first="Remy" last="Robert">Remy Robert</name>
<name sortKey="Russ, Brendan E" sort="Russ, Brendan E" uniqKey="Russ B" first="Brendan E" last="Russ">Brendan E. Russ</name>
<name sortKey="Tan, Jian K" sort="Tan, Jian K" uniqKey="Tan J" first="Jian K" last="Tan">Jian K. Tan</name>
<name sortKey="Thorburn, Alison N" sort="Thorburn, Alison N" uniqKey="Thorburn A" first="Alison N" last="Thorburn">Alison N. Thorburn</name>
<name sortKey="Wong, Connie H" sort="Wong, Connie H" uniqKey="Wong C" first="Connie H" last="Wong">Connie H. Wong</name>
</country>
</tree>
</affiliations>
</record>

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Avenues to autoimmune arthritis triggered by diverse remote inflammatory challenges.

Avenues to autoimmune arthritis triggered by diverse remote inflammatory challenges.

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